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Psychopharmacology > Lecture 15 Pain Syndromes and Analgesics > Flashcards

Lecture 15 Pain Syndromes and Analgesics Flashcards

1
Q

Pain

A

A normal unpleasant physical sensation associated with tissue damage or dysfunction

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2
Q

What are the two major types of pain?

A

Physiological (nociceptive) and chronic (intractable, neuropathic)

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3
Q

Congentical absence of pain…

A

Rare genetic defect in which a person has normal skin sensation but is unable to perceive pain from birth; compound fractures, loss of body parts can go unnoticed

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4
Q

Nociception

A

“noxious perception” the perception of pain

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5
Q

Nociceptor

A

Receptor for stimuli (chemical, mechanical, thermal) that result in pain perception; located on free nerve endings in skin, muscle, organs

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6
Q

Analgesia

A

absence of pain

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7
Q

Anesthesia

A

Absence of all sensory perception

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8
Q

Anesthetic

A

A substance that reduces perception of numerous senses (touch, pain, temperature, pressure)

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9
Q

Analgesic

A

A substance that diminishes the perception of pain

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10
Q

Names some pain syndromes

A 
Lower back pain
Headache /migraine
Cancer-related
Fibromyalgia
Sciatica
Diabetic neuropathy
Shingles
Phantom limb pain
burn pain
Arthritis
Trigeminal neuroalgia
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11
Q

A(delta) fibers

A

Myelinated fibers (20 m/sec) for quick, sharp pain

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12
Q

C fibers

A

Unmyelinated fibers (2 m/sec) for dull, slow pain

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13
Q

Aβ fibers

A

normal mechanical stimuli signals

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14
Q

PN

A

Projection neurons (ascends up to brain); receive pain signals at the dorsal root of the spinal cord

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15
Q

What are the nerve fibers that conduct pain signals?

A

A(delta), C fibers, Projection neurons

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16
Q

What results from tissue damage?

A

Tissue damage causes the release of various chemicals that activate pain fibers, such as histamine, bradykinin (BK), and prostaglandins.

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17
Q

TRP receptors

A

Transient receptor potential (TRP) receptors, including vanilloid receptors (i.e., VR1) are thermosensitive and chemosensitive receptors on free nerve endings.

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18
Q

What activates TRP receptors

A

Activated by heat, changes in pH, capsaicin (chili peppers), wasabi, etc

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19
Q

How does pain arise from demyelination?

A

Accumulation of voltage-sensitive sodium channels (VSSCs) in demyelinated areas of sensory neurons increases ectopic (“out of place”, spontaneous) activity, and hypersensitivity to normal sensations

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20
Q

How does pain occur after severing a nerve?

A

Neuroma – misguided bundle of newly sprouted nerve fibers following nerve cut

Accumulation of VSSCs in neuromas increases ectopic activity, and hypersensitivity to normal sensations

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21
Q

Neuroma

A

Misguided bundle of newly sprouted nerve fibers following nerve cut.

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22
Q

Where does all sensory information enter in the spinal cord?

A

The dorsal horn of the spinal cord.

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23
Q

Where is the reduction of emotional components of pain managed?

A

The amygdala

24
Q

Where does the inhibition of pain signals occur

A

The thalamus

25
Q

Spinal and supraspinal analgesia

A

spinal analgesia is when drugs act at the spine

supraspinal is when drugs act at the brain

26
Q

What are the pain neurotransmitters in the spinal cord?

A

opioid (µ, delta, kappa), 5-HT, and NE

27
Q

What modulates descending pain pathways?

A

NE (from locus coeruleus) and 5-HT (from raphe nuclei) modulate pain in the spinal cord

SSRI, SNRI, NRIs can thus alleviate chronic pain in some patients

28
Q

Name some local anesthetics?

A

Novocaine, lidocaine, cocaine

29
Q

How do local anesthetics work?

A
  • block VSSCs on sensory neurons
  • loss of action potentials results in reduced sensation of pain, touch, pressure, temperature (numbness)
  • must be given locally (i.e., topical subcutaneous injection, epidural)
30
Q

COX

A

Cyclooxygenase (COX) - enzyme that produces prostaglandins which are released from cells after tissue injury; prostaglandins activate pain pathways

31
Q

NSAID

A
  • Non-steroidal anti-inflammatory drugs (NSAIDs) are COX inhibitors
  • aspirin, ibuprofen, naproxen, acetaminophen (Tylenol), prescription COX inhibitors (Vioxx, Celebrex)
32
Q

Synthetic steroids

A

(i.e. hydrocortisone, prednisone) – reduce peripheral inflammation (not via COX inhibition), but long term use is harmful to immune system

33
Q

Anticonvulsants can be used for what type of pain?

A

Neuropathic pain

34
Q

What are the mechanisms of anticonvulsants for pain?

A
  • Inhibition of VSSCs and voltage-sensitive Ca+ channels

- Inhibition of GABA reuptake/metabolism

35
Q

Where do opiates act on?

A

Act primarily on mu (m) opioid receptors located on primary afferent terminals in dorsal horn of spinal cord.

36
Q

What normally activates the mu opioid receptors?

A

normally activated by endorphins and enkephalins

inhibit transmission of pain signals to brain

37
Q

What are some side effects of opioids?

A

side effects include sedation, respiratory depression, constipation, tolerance, dependence, & addiction.

38
Q

What are endocannabinoids generated from?

A

Arachidonic acid (a fatty acid found in the cell membrane) after stimulation of certain neurotransmitter receptors.

39
Q

Cannabinoids are what type of messenger?

A

Act as retrograde messengers to inhibit neurotransmitter release.

40
Q

THC is an agonist at what receptors?

A

THC is an agonist at cannabinoid (CB1) receptors

41
Q

What are 3 synthetic THC and cannabinoids?

A

Sativex, Marinol, Cesamet

42
Q

Why can’t cannabinoids be stored in vesicles?

A

They are highly lipid soluble (therefore cannot be stored in vesicles)

43
Q

What are the 4 phases of a migraine?

A
  • Prodrome
  • Aura
  • Pain phase
  • Postdrome
44
Q

Prodrome

A

Symptoms such as altered mood, fatigue, yawning, excessive sleepiness, craving for certain food, stiff muscles, hot ears, GI problems, etc. appear hours to days before migraine

45
Q

Aura

A

Disturbance of vision just before headache

46
Q

Pain phase

A

Headache on one side of head with nausea, photophobia

47
Q

Postdrome

A

Exhaustion, irritability, depression

48
Q

What are common migraine triggers?

A
  • Estrogen and progesterone
  • Alcohol, chocolate, etc.
  • Stress, physical activity
  • Sight, smells
  • Certain medications
49
Q

What are four types of headaches?

A

Sinus, cluster, tension, migraine

50
Q

Trepenation

A

Medieval treatment

(drilling hole in skull), hot iron to the head, blood letting.

51
Q

What was the first effective medication for migraines?

A

Ergotamine which constricts blood vessels

52
Q

Triptans

A

Sumatriptan (Imitrex), zolmitriptan (Zomig), naratriptan, rizatriptan, eletriptan, almotripan, etc.

53
Q

What are the mechanisms of triptans?

A

Cause vasoconstriction via stimulation of 5-HT1B serotonin receptors on blood vessel walls, also reduce inflammation of vessels by stimulation of 5-HT1D serotonin receptors in brainstem.

54
Q

Phantom limb pain

A

-Tingling, itching, burning, aching, stabbing sensations that appear to emanate from body parts post amputation

55
Q

What was the historical theory for phantom limb pain?

A

Historically, the dominant theory for cause of phantom limb pain was the presence of neuromas that generated nonsense sensations

56
Q

What are todays theory of phantom limb pain?

A
  • maladaptive reorganization of the primary sensory cortex
  • conflict between signals received from the amputated limb (proprioception) and visual information
  • vivid limb position memories that emerge after amputation
57
Q

What are common treatments for phantom limb pain?

A

Common treatments are antidepressants, spinal cord stimulation, vibration therapy, acupuncture, hypnosis, biofeedback, and mirror therapy.

Generally not relieved by opiate analgesics.

Psychopharmacology (17 decks)

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